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Epithelium related deposition of activated complement in Helicobacter pylori associated gastritis

A E Berstad1, P Brandtzaeg, R Stave

  • 1Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), University of Oslo, National Hospital, Norway.

Gut
|February 1, 1997
PubMed

Insights

Helicobacter pylori infection activates complement in vivo, contributing to chronic gastritis. However, the bacteria may evade complement attack in specific gastric locations.

Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiology

Background:

  • The role of complement system activation in Helicobacter pylori-associated gastritis pathogenesis is not fully understood.
  • Complement activation products may deposit in gastric mucosa, potentially contributing to chronic gastritis.

Purpose of the Study:

  • To investigate whether Helicobacter pylori infection activates the complement system in vivo.
  • To examine the mucosal deposition of complement activation products in patients with and without H. pylori infection.

Main Methods:

  • Immunohistochemistry was used to examine gastric tissue sections from H. pylori-infected and uninfected patients.
  • Monoclonal antibodies against activation neoepitopes of C3b and the terminal complement complex (TCC) were employed.
  • Control samples included biopsy specimens from patients with Billroth II gastrectomy.

Main Results:

  • Terminal complement complex (TCC) deposition was observed in various forms of gastritis, including H. pylori-positive, H. pylori-negative, and stump gastritis.
  • Activated C3 was significantly more prevalent on the apical surface of gastric epithelium in H. pylori-infected individuals compared to uninfected ones.
  • Activated C3 was found coating H. pylori near pit openings but rarely within the foveolae.

Conclusions:

  • Local complement activation occurs in chronic gastritis, irrespective of H. pylori infection status.
  • The deposition of activated C3 is more frequent in H. pylori-infected gastric mucosa.
  • H. pylori appears to evade complement attack within the gastric foveolae.
Abstract

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